J Cancer 2019; 10(5):1197-1208. doi:10.7150/jca.28908 This issue

Research Paper

Lyn Kinase Promotes the Proliferation of Malignant Melanoma Cells through Inhibition of Apoptosis and Autophagy via the PI3K/Akt Signaling Pathway

Qianqian Zhang1,2,3, Xianguang Meng1, Guojing Qin1, Xiaotong Xue1,4, Ningning Dang1✉

1. Department of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, China
2. Taishan Medical University, Taian, Shandong Province, China
3. Department of Dermatology, No. 960 Hospital of The Chinese People's Liberation Army, Taian, Shandong Province, China
4. School of Medicine, Shandong University, Jinan, Shandong Province, China

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Citation:
Zhang Q, Meng X, Qin G, Xue X, Dang N. Lyn Kinase Promotes the Proliferation of Malignant Melanoma Cells through Inhibition of Apoptosis and Autophagy via the PI3K/Akt Signaling Pathway. J Cancer 2019; 10(5):1197-1208. doi:10.7150/jca.28908. Available from https://www.jcancer.org/v10p1197.htm

File import instruction

Abstract

Melanoma is a malignant tumor of cutaneous melanocytes that is characterized by high grade malignancy, rapid progression and high mortality. Thus far, its specific etiological mechanism has been unclear. In this study, we discovered that Lyn kinase expression was up-regulated in melanoma tissues and cells. The function of Lyn was determined by knocking down its expression with a lentivirus containing Lyn shRNA and upregulating its expression with pcDNA3.1-Lyn in the melanoma cell lines M14 and A375. The results showed that Lyn knockdown could significantly inhibit the proliferation, migration and invasiveness through its inhibition of apoptosis and autophagy via the PI3K/Akt pathway in melanoma cell lines. This was further confirmed by treatment with PI3K inhibitor BEZ235. Up-regulation of Lyn promoted the expression of p-Akt and Cyclin D1. Additionally, we investigated the effects of Lyn inhibitor Bafetinib on melanoma cells and the results were consistent with Lyn knockdown. Collectively, our results indicated that Lyn plays a carcinogenic role in multiple cellular functions during melanoma development through regulating apoptosis and autophagy via the PI3K/Akt pathway and may be a valuable potential target for the clinical treatment of melanoma.

Keywords: Lyn, melanoma, proliferation, autophagy, PI3K/Akt